The provirus of the Moloney murine sarcoma virus (MSV) contains an MSV-specific transforming sequence (v-mos) whose transforming efficiency can be enhanced by MSV long terminal repeat (LTR) sequences linked either 5 feet or 3 feet. Enhancement of v-mos transformation by LTR sequences linked 3 feet requires only those U3 sequences containing the 73 bp repeat. Promoter sequences and the polyadenylation site derived from unique 5 feet and 3 feet LTR sequences are not required. Althouth v-mos transformation is efficiently enhanced by a 3 feet LTR, c-mos linked to a 3 feet LTR transforms poorly. A sequence approximately 1.2 to kb 5 feet to c-mos has been identified which prevents the enhancement of c-mos transformation by a 3 feet LTR. This sequence apparently blocks the enhancer function of the 73 bp repeat sequence. The human cellular homologue (hu-mos) of mos does not transform NIH3T3 mouse cells even when linked to LTR sequences. Certain recombinants between hu-mos and v-mos containing sequences derived from both parents are able to transform, indicating that under appropriate conditions hu-mos can act as a transforming gene. A dominant gene has been identified from the human pancreatic carcinoma cell line PANC-1. This gene appears to be a member of the family of human sequences related to the ras oncogene band on Kirsten murine sarcoma virus.